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Biomedical subjects

W Fried

Publications and source records attributed to W Fried.

At least 19 recordsLinked to original sources
PubMed2006

Vertical distraction of fibula transplant in a case of mandibular defect caused by shotgun injury.

This case demonstrates the successful aesthetic and functional reconstruction of a complex facial gun-shot injury with extended bone defects and soft tissue destructions using a 3-step procedure. Initially, a reconstruction plate was inserted, later a fibula transplant enabled the basic reconstruction and finally was distructed in a 3rd session. The rationale behind the sequencing of surgical sessions was the extended bony defect and soft-tissue destruction. The main problem in this type of wound is hypoxia or anoxia of the receptor bed for the transplant. A microvascular anastomosized bone transplant is necessary for sufficient oxygen tension in the recipient site. The anatomical dimensional disproportion of the transplanted free fibula graft and the shape of the mandible were corrected prior to the insertion of dental implants by means of vertical distraction.

Bone Plates↗
PubMed2006

[Evaluation of individual ceramic implants made of Bioverit with CAD/CAM technology to reconstruct multidimensional craniofacial defects of the human skull].

BACKGROUND: Restrictions in the bone structure of the craniomandibular region caused by malformation, traumata or malignant tumours are currently of interest in reconstructive oral and maxillofacial surgery. Methods of autologous bone transplantation are well established for reconstruction of those defects. The reconstruction and remodeling of contour-shaping defects is more difficult due to atrophy and resorption of free-transplantable tissues. Artificially induced harmful effects have been reported on harvesting in the donor area. Further available methods of alloplastic reconstruction are computer-assisted design and manufacturing systems (CAD/CAM). The advantages of individual design and fabrication are obvious in the manufacturing of defect-specific implants. MATERIAL AND METHODS: In the present study the application of individual CAD-based reconstructed bioceramic implants made of Bioverit II was evaluated in the region of the facial skull. Clinical results, patient acceptance and the analysis of the postoperative observation period of 30 months are reviewed. RESULTS: Altogether 25 individual Bioverit ceramics were implanted in the facial region. All patients were satisfied with the aesthetic results of the implantations after primary surgery. Three patients developed a need for further correction during the observation period; one implant fracture was observed. CONCLUSION: Finally, it can be stated that the preoperative expenditures in time, experts, technology and fabrication of individual CAD/CAM planned and manufactured implants are justified by the following advantages: fixed volume, reduced operating time, lack of donor morbidity, easy subsequent treatment of the material and the aesthetic results achieved.

Adult↗
PubMed1995

Erythropoietin.

Erythropoietin (Epo), the first growth factor to be discovered, is an endocrine hormone produced by specialized renal cells. The rate of Epo production is determined primarily by the oxygen demands of these renal cells relative to their oxygen supply. However, Epo production is modulated by various hormones, nutritional factors, cytokines, and the integrity of the erythron. Epo interacts with specific receptors found almost exclusively on erythroid progenitors. This interaction results in an expansion of the number of the erythroid progenitor and triggers late committed progenitors to undergo terminal maturation when provided with essential nutrients. Recombinant human Epo (rHuEpo) is commercially available for human use. It is safe, easily administered, and almost universally effective in treating the anemia of patients with renal failure. It has also been successful in treating the anemia of some patients with neoplasms, myelodysplastic syndromes, HIV infection, rheumatoid arthritis, and aplastic anemia. Much remains to be learned about the regulation of Epo production, the physiologic actions of Epo, and how best to use this growth factor in the treatment of anemia.

Anemia↗
PubMed1994

Immunologically mediated aplastic anemia in mice: evidence of hematopoietic stromal injury and injury to hematopoietic stem cells.

Immunologically mediated aplastic anemia (AA) results when lymph node cells (LNC) from C3H/He mice are injected intravenously (i.v.) into H-2 identical CBA/J mice previously given 600 cGy sublethal total-body gamma irradiation (TBI). Previously, we showed that T lymphocytes injure pluripotent hematopoietic stem cells and cause severe pancytopenia and death in 80 to 100% of mice within 3 to 4 weeks, with changes in the bone marrow suggesting stromal injury. The following models were used to study the stroma: (1) Transplantation of femurs from AA mice into normal syngeneic CBA/J mice. After 6 weeks, colony-forming unit-spleen (CFU-S) levels in the femur implants were measured in both AA and control mice (600 cGy TBI only). (2) Development of Dexter long-term bone marrow cultures from AA and control mice, which were used to support hematopoietic bone marrow cells (colony-forming units-granulocyte/macrophage [CFU-GM]) from normal mice. (3) Cellulose ester membranes (CEM) were coated with hematopoietic stroma from AA and control mice and then implanted intraperitoneally (i.p.) into syngeneic CBA/J mice. Six months later, the CEM were removed and analyzed for the presence of trilineal hematopoiesis and bone. Injury to the hematopoietic stroma was documented by the following: (1) Femurs from AA mice had a decreased number of CFU-S compared to controls; (2) Dexter cultures from AA mice formed abnormal stromal layers with a decreased capacity to support CFU-GM from normal donor mice; and (3) CEM coated with stromal cells from AA mice had a decreased capacity to support trilineal hematopoiesis and bone compared to CEM coated with marrow stroma from control mice.

Anemia, Aplastic↗
PubMed1993

Hematopoiesis on cellulose ester membranes. XIII. A combination of cloned stromal cells is needed to establish a hematopoietic microenvironment supportive of trilineal hematopoiesis.

A mixture of stromal cells from murine bone marrow placed upon cellulose ester membranes (CEM) and then implanted intraperitoneally (i.p.) in mice results in a regenerated hematopoietic microenvironment which supports trilineal hematopoiesis. We used this model to study the capacity of 5 cloned murine stromal cell lines of marrow origin to support hematopoiesis in vivo: MBA-1 (fibroblast); MBA-2 (endothelial); MBA-13 (fibroendothelial); 14F1.1 (endothelial-adipose); and 14M1.4 (macrophage).10(7) stromal cells of a single cell line were applied to 1.5 cm2 CEM, which were folded into tubes and implanted i.p. into mice. Similarly, combinations of 4, 3 and 2 stromal cell lines were applied to CEM and implanted i.p. Single lines were implanted into syngeneic hosts of the same murine strain from which the clone was derived and into nude mice. Combinations of stromal cells were implanted only in nude mice to avoid allogeneic incompatibility. CEM implants were removed after intervals of 5 to 36 weeks and examined histologically. 1) Stromal cells of a single phenotype did not develop hematopoiesis. 2) A combination of 4 stromal phenotypes (MBA-1, MBA-2, MBA-13 and 14F1.1) formed a hematopoietic microenvironment supportive of trilineal hematopoiesis and bone. 3) The combination of 14F1.1 (endothelial adipose) + a second stromal phenotype--MBA-1 (fibroblast) or MBA-2 (endothelial) or MBA-13 (fibroendothelial) also supported trilineal hematopoiesis and bone. 4) CEM coated with MBA-13 or MBA-1 developed bone but no hematopoiesis. The endothelial-adipose phenotype appears to be essential to support hematopoiesis but requires other types of stromal cells--fibroblast, fibroendothelial or endothelial phenotype.

Animals↗
PubMed1989

Cyclic thrombocytopenia of apparent autoimmune etiology.

Serial studies were performed in two patients with cyclic thrombocytopenia to investigate the pathogenesis of this disorder. Mean life span of autologous platelets when platelet levels were declining was subnormal (2.4 and 0.8 days), and megakaryocytes were abundant in the bone marrow during thrombocytopenia. Megakaryocyte colony-stimulating activity could not be detected in the serum of either patient at any point of their cycles. In each patient, total platelet-associated IgG varied inversely with platelet levels. Surface platelet-associated IgG was measured only in patient 2 and was significantly elevated (greater than 1,280 IgG molecules per platelet) at all stages of the cycle, even during thrombocytosis. However, the highest values were observed during thrombocytopenia. Platelet-bindable IgG in plasma declined to normal immediately before platelet levels began to rise. IgG eluted from the platelets of this patient reacted strongly with autologous and homologous platelets in contrast to a "mock eluate" prepared from platelets of a normal subject. The eluate from the patient's platelets reacted strongly with immobilized autologous and homologous glycoprotein IIb/IIIa complex and weakly with GPIb but not with isolated GPIIIa alone. In each patient the decline in platelet levels was significantly delayed following administration of intravenous gamma globulin 0.4 g/kg body weight for five days. These findings suggest that platelet-reactive autoantibodies are of pathogenic significance in some patients with cyclic thrombocytopenia.

Adult↗
PubMed1989

Effects of bone marrow transplantation and polyinosinic-polycytidylic acid (poly I:C) on the rescue of animals from busulfan-induced NK suppression.

Repeated injections of busulfan (Bu) in CAF1 mice caused a long-lasting (greater than 16 weeks) decrease in their natural killer (NK) cell activity and impaired their resistance to transplantable lymphoma. Bu-treated mice had fewer spleen cells capable of binding to NK-sensitive YAC-1 target cells and reduced lymphokine-activated killer (LAK) cell activity as compared to normal age-matched controls. In contrast, interleukin 1 (IL-1) and interleukin 2 (IL-2) production were normal. Transplantation of normal bone marrow cells into Bu-treated mice resulted in an elevation of IL-2 production as well as in complete restoration of NK activity, target cell binding, and partial restoration of LAK activity. Resistance to transplantable lymphoma was equal to that of age-matched control mice. Polyinosinic-polycytidylic acid (Poly I:C) treatment resulted in immunomodulation in both control and Bu-pretreated mice. Twenty-four hours after Poly I:C injection, control and Bu-treated mice had higher levels of NK activity than did normal age-matched control mice, but the NK activity of Poly I:C/Bu-treated mice remained significantly lower than that of Poly I:C/control mice. The super-normal levels of NK activity in control and Bu-treated mice following Poly I:C administration were attributable, in part, to endogenous LAK activity. The generation of splenic LAK cells in vitro and target binding cells, which were reduced in Bu-pretreated mice, normalized following treatment with Poly I:C. Poly I:C treatment caused an increase in both IL-1 and IL-2 production in control and Bu-pretreated mice and in the ability of the treated mice to reject transplanted lymphoma cells. These results suggest that repeated injections of Bu decrease NK and LAK activity, but do not eliminate NK and LAK precursor cells. Thus, treatment with agents that increase IL-2 and/or interferon production can activate these cells to become effective killers and counter the long-lasting immunosuppressive effects of chemotherapy.

Animals↗
PubMed1989

Hematopoiesis on cellulose ester membranes. XI. Induction of new bone and a hematopoietic microenvironment by matrix factors secreted by marrow stromal cells.

Cellulose ester membranes (CEM) were coated with stromal cells from bone marrow (BM) or bone and implanted intraperitoneally (IP) in CAF1 mice for intervals of 1 to 6 months. Previous studies indicated that matrix factors [glycoproteins (GPs), proteoglycans (PGs), and glycosaminoglycans (GAGs)] were secreted by the regenerating stromal cells and adsorbed by the CEM. After 1 to 6 months, the CEMs were removed, scraped free of adherent cells, and irradiated in vitro with 40 Gy. The scraped and irradiated CEMs were then reimplanted IP or subcutaneously (SC) for periods of 1 to 6 months in secondary syngeneic murine hosts. They were then removed for histologic study. CEMs reimplanted in SC sites developed bone and hematopoiesis as early as 1 month after implantation. Maximum hematopoiesis and bone formation was observed after 3 months. CEMs coated during the initial implantation with bone-derived stromal cells contained more bone and hematopoietic cells than did CEMs coated with marrow-derived stromal cells after SC implementation. Neither the CEMs coated with bone stromal cells nor those coated with marrow stromal cells developed new bone or trilineal hematopoiesis after being implanted IP. A few CEMs contained small foci of granulopoiesis only. We conclude that noncellular matrix substances deposited on CEMs by bone, and to a lesser degree by marrow cells, can induce prestromal cells in the SC tissues to produce a microenvironment suitable for trilineal hematopoiesis.

Animals↗
PubMed1988

Effect of indomethacin and of prostaglandins on extrarenal erythropoietin production in rats.

Indomethacin elevates the plasma erythropoietin titer of hypoxic anephric rats and probably does so by increasing extrarenal erythropoietin production. Because indomethacin is a potent cyclooxygenase inhibitor, we postulated that it alters extrarenal erythropoietin production via its effects on tissue prostaglandin levels. Studies were, therefore, performed to determine the effects of indomethacin on hepatic prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) titers. Indomethacin significantly decreased the PGF2 alpha level but its effects on the PGE2 level were, in most experiments, insignificant. We next studied the effects of infusing PGF2 alpha and PGE2 on the plasma erythropoietin levels of hypoxic rats. PGF2 alpha significantly reduced the plasma erythropoietin titer of anephric rats and neutralized the effect of indomethacin when both substances were administered. PGE2 infusion, on the other hand, did not significantly affect the plasma erythropoietin level of anephric rats. The data support the conclusion that PGF2 alpha is a potent inhibitor of extrarenal erythropoietin production, and that indomethacin enhances the rate of extrarenal erythropoietin production by reducing the PGF2 alpha titer in the liver.

Animals↗
PubMed1986

Busulfan and chloramphenicol induced T cell lymphoma: cell surface characteristics and functional properties.

We report the immunological studies on three transplantable lymphoma lines that developed when CAF1 mice were injected with busulfan and chloramphenicol. The lymphoma cells displayed Thy-1.2, brain associated antigen, and H-2d alloantigen. They were negative for surface IgM and Ia antigens. Expression of T cell differentiation antigens differed among the three lines. The 508 tumour line displayed only Thy-1.2: 408 tumour line displayed Thy-1.2, Lyt-2.2 and TL; and 808 tumour line was positive for Thy-1.2, Lyt-1.2, Lyt-2.2 and TL antigens. We established in vitro culture lines from 508 and 808 lymphoma cells. The lymphoma cells did not respond to mitogens and antigens. The splenic cells from mice bearing 508 or 808 had decreased phytohaemagglutinin (PHA), concanavalin A (Con A) and mixed leucocyte responses (MLR). When mitomycin-C treated lymphoma cells from the tumour bearing mice were cocultured with normal splenic mononuclear cells, the 808 lymphoma cells suppressed the mitogenic responses of the normal cells more profoundly than 508 lymphoma cells. Adherent cells from both tumours suppressed the Con A responses of normal spleen cells. Cells from in vitro 508 or 808 cell lines had no effect on mitogenic responses of normal cells. Plasma from tumour bearing mice, but not the supernatants taken from cultures of these lymphoma cells, suppressed the mitogenic responses of normal lymphocytes. Spleen cells from normal CAF1 mice responded in mixed leucocyte tumour reactions (MLTR) when cocultured with lymphoma cells. Mice immunized with mitomycin-C treated tumour cells had greater response. Responder cells taken from mice with established 508 or 808 tumors had suppressed MLTR responses. Although prior immunization with tumor antigen increased the MLTR response, injection of live tumour cells into immunized mice resulted in a more rapid tumour growth and suppression of MLTR response.

Animals↗
PubMed1985

Busulfan-induced suppression of natural killer cell activity.

The effect of repeated injections of busulfan, an alkylating agent, on immune response of CAF1 mice was studied. A single injection of busulfan or acetone (vehicle to solubilize busulfan) acutely suppressed mitogenic and allogenic responses that normalized at two weeks. Repeated injections of busulfan (four injections), on the other hand, showed a transient suppression of the mitogenic responses. Natural killer (NK) activity during the first ten days after busulfan or acetone injections remained normal. NK activity diminished significantly after two injections of busulfan, remained low after four injections, and did not recover within four months of rest. Prolonged suppression of NK activity may be implicated as playing a role in the emergence of T-cell lymphomas in mice injected with busulfan.

Animals↗
PubMed1985

Late effects of chemotherapy on hematopoietic progenitor cells.

Residual damage to marrow function has been observed in cyclophosphamide-treated or irradiated mice following recovery of marrow hematopoietic stem cells (CFU-S) and peripheral blood counts to pretreatment levels. Residual damage is evidenced by less rapid recovery of marrow CFU-S and blood counts following subsequent exposure to sublethal irradiation. Mice treated with busulfan also demonstrate residual marrow damage as evidenced by incomplete recovery of marrow CFU-S to pretreatment levels. We report here on studies to determine whether the residual marrow damage after radiation, cyclophosphamide, or busulfan therapy is exerted on the hematopoietic stroma's ability to support CFU-S proliferation (HS-P) or on the repopulating potential of the CFU-S per se. HS-P function is determined by measuring the ability of femora implanted subcutaneously into syngeneic mice to support the growth of host CFU-S. Evidence is presented to show that this function depends on fixed (nonmigrating) cells in the marrow environment. The repopulating potential of CFU-S is determined by measuring the rate of regeneration of marrow CFU-S after transplantation into lethally irradiated mice. The results of these studies indicate that exposure to 950 rad, busulfan, or cyclophosphamide all cause damage to the HS-P that persists for at least six weeks after therapy. After cyclophosphamide therapy, but not after exposure to the other two agents, HS-P function continues to improve six weeks after therapy and eventually reaches pretreatment levels. Only in busulfan-treated mice was the residual damage to the CFU-S repopulating capacity significantly more marked than damage to HS-P function.

Animals↗